Relatively little is known about the neurobiology of insomnia, despite its wide prevalence and broad medical impact. Although much is still to be learned about the pathophysiology of the disorder, identification, systematic assessment, and appropriate treatment are clearly beneficial to patients. Recent research, using quantitative EEG, polysomnography (PSG), multiple sleep latency test (MSLT) and neuroimaging techniques, suggests that some broad areas can be identified as possible pathophysiological models. Sleep-wake homeostat model hypothesizes a failure in homeostatic regulation of sleep, an attenuated increase in sleep drive with time awake, and/or defective sensing of sleep need. Circadian clock model hypothesizes a dysfunctional circadian clock, resulting in changes in the timing of sleep-wake propensity that are incompatible with normal sleep. Intrinsic sleep-wake state mechanism model suggests that abnormal function of insomnia comprises the systems responsible for expression of the sleep states themselves. Extrinsic over-ride mechanism (stress-response) model suggests that insomnia reflects the consequences of overactivity of one of the systems considered "extrinsic" to normal sleep-wake control. Many current therapies for insomnia are based on these physiological models. Several attempts have been made to create a physiological model that would explain this disorder and could be used as a foundation for treatment. However, it appeared that no model can fully explain and clarify all aspects of insomnia. Future research should be necessary to expand our knowledge on the biological dimensions of insomnia.
Circadian Clocks ; Electroencephalography ; Humans ; Neurobiology ; Neuroimaging ; Polysomnography ; Prevalence ; Sleep Initiation and Maintenance Disorders

No abstract available.
Organization and Administration* ; Psychotherapy*

No abstract available.
Movement Disorders* ; Prevalence*

No abstract available.
Organization and Administration* ; Psychotherapy*

The most common pathogen of respiratory tract infection among school-age children and adolescents is Mycoplasma pneumoniae, which causes clinical manifestations of pneumonia, acute asthmatic attack, pharygitis, and tonsilitis. It can also cause extrapulmonary infections that involves skin, the nervous system, the digestive system, the cardiovascular system, and the hematopoietic system. It is reported that the central nervous system symptoms may occur in 0.1% to 7% of patients hospitalized with Mycoplasma pneumoniae infection. Direct invasion, toxin, immune-mediated, and vascular phenomenon have been proposed for the etiology of the neurological manifestations. We have experienced a six-year-old male patient with Mycoplasma pneumoniae pneumonia who had complained of both leg pains and immobility two weeks after the onset of pneumonia, which was confirmed as peripheral neuropathy of Guillain-Barr syndrome. Three weeks after the disease-onset, altered consciousness and seizure attacks developed and intravenous immunoglobulins infused under the impression of encephalitis induced by Mycoplasma pneumoniae infection. He showed complete recovery of running and mentality five months after the disease-onset. We herein report a case of Mycoplasma pneumoniae pneumonia complicated with Guillain-Barr Syndrome and encephalitis about 2 or 3 weeks after the disease onset with a review of literatures.
Adolescent ; Cardiovascular System ; Central Nervous System ; Child ; Consciousness ; Digestive System ; Encephalitis* ; Guillain-Barre Syndrome* ; Hematopoietic System ; Humans ; Immunoglobulins ; Immunoglobulins, Intravenous ; Leg ; Male ; Mycoplasma pneumoniae* ; Mycoplasma* ; Nervous System ; Neurologic Manifestations ; Palatine Tonsil ; Peripheral Nervous System Diseases ; Pneumonia* ; Pneumonia, Mycoplasma* ; Respiratory Tract Infections ; Running ; Seizures ; Skin

PURPOSE:We investigated the production of oxygen hydroxyl radicals in the striatum of neonatal rat brain after intrastriatal injection of dopamine (DA) and the effect of growth hormone (GH) on the apoptosis of striatal neurons injured by hypoxia-ischemia. METHODS:The extracellular striatal levels of 2,3-dihydroxybenzoic acid (DHBA) and 2,5-DHBA as indicators of hydroxyl radical(OH-) production were measured by in vivo microdialysis in the striatums of 7 day-old newborn rats (n=10) after direct intrastriatal infusion of dopamine hydrochloride (1.0 micromol/microL). The samples of perfused artificial cerebrospinal fluid (CSF) were collected every 10 minutes interval. The levels of DA, 2,3-DHBA and 2,5-DHBA of CSF were analysed by HPLC (high performance liquid chromatography). Also, the brains were removed at 24 hour after hypoxic-ischemic injury by Rice-Vannucci method. The coronal sections (12 micrometer) of paraffin-fixed brains were stained by TUNEL (terminal transferase-mediated dUTP nick-end-labelling) technique, and the neuronal cells undergoing apoptosis in the striatum were observed by fluorescent microscopy and compared between GH-treated (50 mg/kg, Dong-Ah Pharmacy Co.) and saline-treated rats. RESULTS:The extracellualr striatal levels of 2,3-DHBA and 2,5-DHBA increased abruptly in the first 10 minutes samples after intrastriatal injection of DA. After then, the levels declined slowely. The levels of striatal extracelluar 2.3-DHBA increased up to 621.8+/-508.7% of basal levels (P<0.05), and the levels of 2.5-DHBA increased up to 262.8+/-198.1% of basal levels (P<0.05). GH reduced markedly the number of apoptotic neuronal cells in the striatum after hypoxic-ischemic brain injury. CONCLUSION: The level of hydroxyl radicals increased abruptly after intrastriatal injection of DA and GH reduced markedly the number of apoptotic neuronal cells in the striatum after hypoxic-ischemic brain injury.
Animals ; Apoptosis* ; Brain Injuries ; Brain* ; Cerebrospinal Fluid ; Chromatography, High Pressure Liquid ; Dopamine* ; Growth Hormone* ; Humans ; Hydroxyl Radical* ; In Situ Nick-End Labeling ; Infant, Newborn* ; Microdialysis ; Microscopy ; Neurons* ; Oxygen ; Pharmacy ; Rats*

OBJECTIVE: Panic disorder has been suggested to be divided into the respiratory and non-respiratory subtypes in terms of its clinical presentations. The present study aimed to investigate whether there are any differences in treatment response and clinical characteristics between the respiratory and non-respiratory subtypes of panic disorder patients. METHODS: Among the 48 patients those who completed the study, 25 panic disorder patients were classified as the respiratory subtype, whereas 23 panic disorder patients were classified as the non-respiratory subtype. All patients were treated with escitalopram or paroxetine for 12 weeks. We measured clinical and psychological characteristics before and after pharmacotherapy using the Panic Disorder Severity Scale (PDSS), Albany Panic and Phobic Questionnaire (APPQ), Anxiety Sensitivity Index-Revised (ASI-R), State-Trait Anxiety Inventory (STAI-T, STAI-S), Hamilton Anxiety Rating Scale (HAM-A), and Hamilton Depression Rating Scale (HAM-D). RESULTS: The prevalence of the agoraphobia was significantly higher in the respiratory group than the non-respiratory group although there were no differences in gender and medication between the two groups. The respiratory group showed higher scores on the fear of respiratory symptoms of the ASI-R. In addition, after pharmacotherapy, the respiratory group showed more improvement in panic symptoms than the non-respiratory group. CONCLUSION: Panic disorder patients with the respiratory subtype showed more severe clinical presentations, but a greater treatment response to SSRIs than those with non-respiratory subtype. Thus, classification of panic disorder patients as respiratory and non-respiratory subtypes may be useful to predict clinical course and treatment response to SSRIs.
Agoraphobia ; Anxiety ; Citalopram ; Classification ; Depression ; Drug Therapy ; Humans ; Panic ; Panic Disorder* ; Paroxetine ; Prevalence ; Surveys and Questionnaires ; Serotonin Uptake Inhibitors ; Treatment Outcome

OBJECTIVE: This study was aimed to compare the efficacy and tolerability of milnacipran and sertraline treatment in patients with major depressive disorder and to evaluate the relationships between beta-adrenergic receptor responsiveness and depressive mood states. METHODS: Fifty three patients who had a diagnosis of major depressive disorder according to the DSM-IV and showed scores of 17 or more on the 17-item Hamilton Rating Scale for Depression (HAM-D) were randomly assigned to either milnacipran or sertraline treatment group. Each patient received 8 weeks of antidepressant treatment with one of the two drugs. Efficacy was assessed using the HAM-D, Beck Depression Inventory (BDI), Montgomery and Asberg Depression Rating Scale (MADRS) and Clinical Global Impression (CGI). Twenty normal control subjects who had no history of psychiatric and major medical illness and were matched with the depressed patients considering age, sex and body mass index were recruited for the comparison of beta-adrenergic receptor responsiveness between depressed patients and normal control subjects. We measured beta-adrenergic receptor density, lymphocyte cAMP ratio (ratio of isoproterenol-stimulated cAMP/basal cAMP), and receptor affinity (Kd) in all subjects. We also investigated beta-adrenergic receptor responsiveness before and after treatment in depressed patients. RESULTS: Twelve patients in milnacipran group and 15 patients in sertraline group were completed this study. In all assessment scales for depression, we found significant decrease in depression severity in both milnacipran and sertraline groups. Both of the two drugs proved equally effective for reduction of the overall symptoms of depression throughout the treatment period. And there were significant differences in the means of Kd values between control subjects and depressed patients before treatment. We found a significant negative correlation between Kd values and BDI scores. After treatment with either milnacipran or sertraline, cAMP ratio (4.8+/-1.6 vs 5.7+/-2.5, p=0.095) and Kd value (65.6+/-11.9 vs 74.6+/-7.8, p=0.066) tended to increase, but there was no significant difference in beta-adrenergic receptor responsiveness between milnacipran and sertraline group. CONCLUSION: Both milnacipran and sertraline were not different in the clinical efficacy in major depressive disorder. In depressed patients, beta-adrenergic receptor responsiveness is reduced and both milnacipran and sertraline antidepressants tended to increase beta-adrenergic receptor responsiveness.
Antidepressive Agents ; Body Mass Index ; Depression ; Depressive Disorder, Major* ; Diagnosis ; Diagnostic and Statistical Manual of Mental Disorders ; Humans ; Lymphocytes ; Sertraline* ; Weights and Measures

OBJECTIVES : The present study aimed to compare anxiety sensitivity among anxiety disorder groups, and to examine the relationships between lower-order factors of anxiety sensitivity and each anxiety disorder. METHODS : Three hundred and twenty four normal control subjects and 212 patients with anxiety disorders were enrolled in this study. All subjects completed a psychometric assessment package including the Korean Anxiety Sensitivity Index-Revised (ASI-R) test. Statistical analysis of the two groups was performed using the Mann-Whitney U test, and comparison of anxiety sensitivity amongthe anxiety-disorder groups (panic disorder-PD, general anxiety disorder-GAD, social phobia- SP, obsessive-compulsive disorder-OCD) was investigated using Kruskal-Wallis test. RESULTS : All anxiety disorder groups showed higher total scores of the ASI-R than did the normal control group (Z=-13.724, p<.001), and the mean total score of the ASI-R in the panic disorder group was the highest among the anxiety disorder groups. The mean score of each lower-order factor of the ASI-R in each anxiety disorder group was higher than that of the normal control group and there were statistically significant differences in fear of cardiovascular symptoms (PD,GAD>SP,OCD), fear of respiratory symptoms (PD>GAD, SP,OCD), and fear of publicly observable anxiety reactions (SP>PD,OCD) among the anxiety disorder groups. CONCLUSION : These results suggest that anxiety sensitivity reflects vulnerability to anxiety disorders, and that lower-order factors of the ASI-R may help in the differential diagnosis of anxiety disorders.
Anxiety ; Anxiety Disorders ; Diagnosis, Differential ; Humans ; Panic Disorder ; Psychometrics

OBJECTIVES : The present study aimed to compare anxiety sensitivity among anxiety disorder groups, and to examine the relationships between lower-order factors of anxiety sensitivity and each anxiety disorder. METHODS : Three hundred and twenty four normal control subjects and 212 patients with anxiety disorders were enrolled in this study. All subjects completed a psychometric assessment package including the Korean Anxiety Sensitivity Index-Revised (ASI-R) test. Statistical analysis of the two groups was performed using the Mann-Whitney U test, and comparison of anxiety sensitivity amongthe anxiety-disorder groups (panic disorder-PD, general anxiety disorder-GAD, social phobia- SP, obsessive-compulsive disorder-OCD) was investigated using Kruskal-Wallis test. RESULTS : All anxiety disorder groups showed higher total scores of the ASI-R than did the normal control group (Z=-13.724, p<.001), and the mean total score of the ASI-R in the panic disorder group was the highest among the anxiety disorder groups. The mean score of each lower-order factor of the ASI-R in each anxiety disorder group was higher than that of the normal control group and there were statistically significant differences in fear of cardiovascular symptoms (PD,GAD>SP,OCD), fear of respiratory symptoms (PD>GAD, SP,OCD), and fear of publicly observable anxiety reactions (SP>PD,OCD) among the anxiety disorder groups. CONCLUSION : These results suggest that anxiety sensitivity reflects vulnerability to anxiety disorders, and that lower-order factors of the ASI-R may help in the differential diagnosis of anxiety disorders.
Anxiety ; Anxiety Disorders ; Diagnosis, Differential ; Humans ; Panic Disorder ; Psychometrics